Abstract
High-salt diet-induced cardiac hypertrophy and fibrosis are associated with increased reactive oxygen species production. Transient receptor potential vanilloid type 1 (TRPV1), a specific receptor for capsaicin, exerts a protective role in cardiac remodeling that resulted from myocardial infarction, and peroxisome proliferation-activated receptors δ (PPAR-δ) play an important role in metabolic myocardium remodeling. However, it remains unknown whether activation of TRPV1 could alleviate cardiac hypertrophy and fibrosis and the effect of cross-talk between TRPV1 and PPAR-δ on suppressing high-salt diet-generated oxidative stress. In this study, high-salt diet-induced cardiac hypertrophy and fibrosis are characterized by significant enhancement of HW/BW%, LVEDD, and LVESD, decreased FS and EF, and increased collagen deposition. These alterations were associated with downregulation of PPAR-δ, UCP2 expression, upregulation of iNOS production, and increased oxidative/nitrotyrosine stress. These adverse effects of long-term high-salt diet were attenuated by chronic treatment with capsaicin. However, this effect of capsaicin was absent in TRPV1−/− mice on a high-salt diet. Our finding suggests that chronic dietary capsaicin consumption attenuates long-term high-salt diet-induced cardiac hypertrophy and fibrosis. This benefit effect is likely to be caused by TRPV1 mediated upregulation of PPAR-δ expression.
Highlights
Left ventricular hypertrophy is an adaptive response of the heart to hypertension or cardiovascular disease
To determine the function of TRPV1 channels in cardiomyocytes, we examined the intracellular free calcium capsaicin stimulation caused acomnacreknetdraitniocrnea([sCe ao2f+[]Ci)a. 2A+c]iuitne cultured cardiomyocytes (Figure 1(c))
This effect of capsaicin was absent in TRPV1−/− mice on a high-salt diet (P > 0.05). Other echocardiographic parameters such as fractional shortening (FS), left ventricular end-systolic diameter (LVESD), and left ventricular posterior wall (LVPW) have shown the same tendency. These results demonstrated that high-salt diet impairs cardiac function, which can be attenuated by simultaneous administration of capsaicin through the impact on TRPV1
Summary
Left ventricular hypertrophy is an adaptive response of the heart to hypertension or cardiovascular disease. Our previous studies showed that TRPV1 activation by dietary capsaicin improved endothelium-dependent vasorelaxation and regulated blood pressure in rats [9] and prevented high-salt diet-induced hypertension in mice [10, 11]. Huang and his colleagues reported that TRPV1 plays a protective role in cardiac remodeling that resulted from myocardial infarction [12]. It remains unknown whether chronic activation of TRPV1 via dietary capsaicin could attenuate cardiac hypertrophy induced by long-term high-salt diet. We hypothesize that TRPV1 activation by capsaicin might prevent cardiac damage induced by oxidative stress through PPAR-δ upregulation
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